Saturday, June 19, 2010

Although USDA-APHIS presented paperwork asking for a higher bovine spongiform encephalopathy (BSE) status from the World Organization for Animal Health (OIE), the U.S. did not get a change in status.

The U.S. remains a controlled BSE risk status, in the same category as Canada and Mexico.

Under OIE regulations, there are three BSE risk categories - negligible, controlled and undetermined risk.

Cindy Ragin, press relations at USDA-APHIS, said she did not know why the U.S. was not upgraded in status, but said they did send in paperwork requesting the upgrade.

At the 78th OIE annual general session held in Paris from May 23-28, world delegates decided on the member countries' BSE status, Ragin said. There are 176 countries who are members of the OIE.

Korea received an upgrade to a controlled risk status from a previous status as an undetermined risk.

Controlled risk status is granted to countries where surveillance is adequate and there are measures in place to prevent an outbreak of the disease, even though some cases of BSE are still found, according to the OIE.

However, Korea's livestock producers are still suffering from an outbreak of Foot and Mouth Disease (FMD). Korea's last outbreak of FMD was reported in March 2010 and involved a pig. Some 317 cattle and 1,223 pigs on the farm were slaughtered, according to the OIE.

FMD outbreaks are occurring in other countries in the Far East including Japan and Hong Kong. There have also been recent outbreaks of FMD in South Africa, Mongolia and Egypt.

Key work of the Assembly The Delegates approved the new list of countries and zones that had applied for official OIE recognition of their status with respect to one or more of four priority diseases: bovine spongiform encephalopathy (BSE), foot and mouth disease, contagious bovine pleuropneumonia (CBPP) and rinderpest. With regard to BSE, the OIE newly recognised India and Peru as having a “negligible risk” status, while the Republic of Korea and Panama were recognised as having a “controlled BSE risk status”.

On the proposed changes to OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animals

20

CHAPTER 2.4.6: BOVINE SPONGIFORM ENCEPHALOPATHY

General comments

The changes proposed are generally welcomed by the EU. However, some specific comments detailed below should be taken into account for the final revised version to be adopted in the next General Session.

Specific comments

LINE 13: The words "and possibly spontaneous" should be added as follows: "... suggesting that earlier, undetected indigenous and possibly spontaneous cases may have occurred."

LINE 31: The EU would argue for the re-instatement of the deleted phrase [before, or without, the recognition] since fallen stock in particular could be showing some clinical signs which went unrecognised. As written, it applies more to the active screening of the healthy slaughter population.

Line 228: Replace: "All currently recognized forms of BSE (C, H and L-Type) are detectable by these methods." with: "Classical BSE is recognized by all these methods, while a complete evaluation of the approved BSE rapid tests on atypical forms (C, H and L-Type) was never carried out".

CONTROL OF HAZARDS OF AQUATIC ANIMAL HEALTH HAZARDS AND PUBLIC HEALTH IMPORTANCE IN AQUATIC ANIMAL FEEDS EU

comment

The EU would agree with the proposed amendments. Nevertheless, the proposed chapter would benefit of the following amendments:

1) With regard to Article 4.5.4., point 4 on "Good practices", the following rewording is proposed for the first sentence (highlighted): Where national guidelines exist, good aquaculture practices and good manufacturing practices (including good hygienic practices) should be followed. Countries without such guidelines are encouraged to develop them or to take already available or existing guidelines on board.

2) With regard to Article 4.5.4. point 5 on "relationship between prions and aquatic animal species", it must be highlighted that in a recent publication by Salta et al. (2009) it was reported that Gilthead Sea Bream developed TSE-like pathologies after having been force fed with BSE agent and Scrapie agent respectively. The PrPTSE found in Sea Bream was Sea Bream PrP and not residual PrPBSE or PrPSc. Therefore, there is now evidence showing that TSEs can be potentially transmitted from cattle or sheep to fish. The TSE like pathology was induced after force feeding high quantities of BSE and Scrapie agent. It is yet unknown, whether transmission would occur if more realistic doses of exposure were used. In other words, the “height” of the so called “species barrier” for transmission of PrPTSE from mammals to fish is unknown. However, given the new findings, we suggest that the relevant paragraph is amended to say that there may be a potential risk if terrestrial animal by-products were used as ingredients in aquatic animal feed with respect to prion diseases.

3) With regard to Article 4.5.4., point 11 on "Design and management of inspection programmes" we propose the following wording for the second sentence (highlighted):

Operators in the feed and feed ingredients business and other relevant industries should implement procedures to ensure compliance with regulatory standards for harvest, handling, storage, processing, distribution and use of feed and feed ingredients. Operators have the primary responsibility for implementing systems for process quality control. Where such systems are applied, the Competent Authority should verify that they meet all regulatory requirements. Article 4.5.1. Introduction

IF the truth were known (and it's not like I have not been trying), the USA, Canada, and Mexico (there are other Countries too), should all be listed in this new TSE prion trader friendly atmosphere as ''undetermined risk''. Because USDA et al have absolutely no idea. The ideology of only the UK BSE theory and there from only imported MBM and feed, to ignore the fact that the continuous rendering technology was developed and the USDA got the UK to use it first, some five years before the USA started using the same technology, and then the fact of all the different TSE in different species here in North America, and different strains there from, to continue to believe in only the imported factor of feed and animals, and not take seriously the _home grown_ factor, from tainted _home grown TSE tainted feed_, from the same type rendering technology, is like sticking your head in a hole in the ground and hoping for the best. kind of like what BP did in the Gulf of Mexico. But for the OIE to continue to go by this decades old science on BSE, and continue to ignore the risk factors from other strains of BSE, and other TSE in other species, when scientist from around the globe continue to wave flags of concern, to continue this ignorance is dangerous for human and animal health. But typical for the OIE and the USDA in reference to the Transmissible Spongiform Encephalopathy disease. Both the USDA and the OIE have ignored these documented risk factors for years, even decades, simply for trading purposes. The USDA et al until 2003 when the first documented case of c-BSE was documented in Washington State, the USDA had nothing to do with countries that had BSE. Until that cow old Luther capped in Washington, then the shoe was on the other foot. The USDA and the OIE after that literally changed the rules and regulations on BSE that had been in place for almost a decade trying to eradicate it all around the globe before it mutated, by doing away with the BSE GBR risk assessments and ignoring them, and implementing the infamous force fed USDA BSE MRR policy (all this is explained below in the source reference). But two mad cows sat on ice while all this political science was taking place for 7 months. One finally confirmed thanks to the OIG and the Honorable Phyllis Fong, and the other could not be confirmed due to the fact in had been improperly stored for 4 MONTHS, before testing. Kind of like the other stumbling and staggering mad cow in Texas that got away, went straight to be rendered for pet food, without NO TSE prion test at all. I could go on, about the healthy brains, from healthy cows, cows they knew did not have BSE, submitted for the infamous 2004 Enhanced BSE surveillance and testing program, or the other 9,200 brains they only used IHC testing, the least likely to find BSE. Sadly, once they did start documenting BSE back to back, they shut it down, said that was enough, let's cancel this right here in it's tracks, and we have heard nothing since, like the USA has now become immune to any TSE in any bovine. ;

When the OIE and the USDA et al collaborated to make legal the trading of Transmissible Spongiform Encephalopathy, when they did away with the BSE GBR risk assessments, where the USA, Canada, and Mexico were categorized as BSE GBR III. please see ;

EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.

YET, in 2010, tons and tons of banned mad cow protein are still in commerce here in the USA, scientific studies are being misconstrued and manipulated by ARS USDA, which are still going by TSE science that is decades old, while refusing to acknowledge new scientific studies, and FOIA requests are still being held up by the USDA et al on these urgent matters (see source related materials below). CJD of unknown phenotype, in victims that are getting younger, with longer clinical course from first onset of symptoms to death are occurring, in fact, sporadic CJD is still rising, where the TSEs in the different species are mutating here in the USA, and we still have this same dog and pony show by the OIE and USDA et al. IF you go back and look at the Countries that went by these OIE BSE guidelines, most all came down with BSE. I have said it before, I was say it again now, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization. ...TSS

An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.

WASHINGTON (AP)--The U.S. Department of Agriculture acknowledged Aug. 17 that its testing options for bovine spongiform encephalopathy were limited in 9,200 cases despite its effort to expand surveillance throughout the U.S. herd.

In those cases, only one type of test was used--one that failed to detect the disease in an infected Texas cow.

The department posted the information on its website because of an inquiry from The Associated Press.

Conducted over the past 14 months, the tests have not been included in the department's running tally of BSE tests since last summer. That total reached 439,126 on Aug. 17.

"There's no secret program," the department's chief veterinarian, John Clifford, said in an interview. "There has been no hiding, I can assure you of that."

Officials intended to report the tests later in an annual report, Clifford said.

These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC.

In the Texas case, officials had declared the cow free of disease in November after an IHC test came back negative. The department's inspector general ordered an additional kind of test, which confirmed the animal was infected.

Veterinarians in remote locations have used the preservative on tissue to keep it from degrading on its way to the department's laboratory in Ames, Iowa. Officials this year asked veterinarians to stop using preservative and send fresh or chilled samples within 48 hours.

The department recently investigated a possible case of BSE that turned up in a preserved sample. Further testing ruled out the disease two weeks ago.

Scientists used two additional tests--rapid screening and Western blot--to help detect BSE in the country's second confirmed case, in a Texas cow in June. They used IHC and Western blot to confirm the first case, in a Washington state cow in December 2003.

"The IHC test is still an excellent test," Clifford said. "These are not simple tests, either."

Clifford pointed out that scientists reran the IHC several times and got conflicting results. That happened, too, with the Western blot test. Both tests are accepted by international animal health officials.

""These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."

THIS WAS DONE FOR A REASON!

THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS

USDA 2003

We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back. Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.

snip.............

Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test. There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.

Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.

snip...

FULL TEXT;

Completely Edited Version PRION ROUNDTABLE

Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado

2005

=============================

CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006

The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.

The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end

LET US LOOK AT AUSTRALIA, AND THE BSE RISK ASSESSMENT THE O.I.E. ASK THEM ABOUT IN 2009. IF YOU LOOK AT THESE QUESTIONS, THE USA HAS FAILED AT EVERY ASPECT OF THE QUESTIONNAIRE SET FORTH BY THE O.I.E. FOR AUSTRALIA IN 2009.

AUSTRALIAN QUESTIONNAIRE TO ASSESS BSE RISK

Introduction

Acceptance of a submission from an applicant country for an assessment of BSE risk is based on the provision of comprehensive data and supporting evidence from the Competent Authority over the five areas listed below. In general, the data requirements are consistent with those of Chapter 11.6 – Bovine Spongiform Encephalopathy of the World Organisation for Animal Health (OIE) Terrestrial Animal Health Code, 2009.

A risk assessment to determine the BSE risk status of the cattle population and whether the beef and beef products from a country represent a risk to the health of Australian consumers will be undertaken by Food Standards Australia New Zealand (FSANZ). This document sets out the criteria under the five areas that will be examined to determine BSE risk. Applicant countries should also refer to the documents explaining the assessment process (link) and the requirements for the importation of beef and beef products for human consumption (link).

Countries should note that as part of the assessment, verification of in-country control measures may be undertaken by in-country inspection and the results of any such inspections will be considered prior to completing the country assessment. Countries will be required to provide an annual update report by 31 January to the Australian BSE Food Safety Assessment Committee (the Committee) as described in Section 5. Countries are also required to report to the Committee, within 24 hours, any exceptional developments in regard to the countries BSE status e.g. identification of the first indigenous case of BSE.

TERRESTRIAL ANIMAL HEALTH STANDARDS COMMISSION FEBRUARY 2010 REPORT CHAPTER 1.6. STATUS FOR OIE LISTED DISEASES: PROCEDURES FOR SELF DECLARATION AND FOR OFFICIAL RECOGNITION BY THE OIE

Article 1.6.1.

General principles Members may wish to make a self declaration as to the freedom of a country, zone or compartment from an OIE listed disease. The Member may inform the OIE of its claimed status and the OIE may publish the claim. Publication does not imply endorsement of the claim. The OIE does not recognise publish self declaration for bovine spongiform encephalopathy (BSE), foot and mouth disease (FMD), rinderpest and contagious bovine pleuropneumonia (CBPP). Members may request official recognition by the OIE as to: 1. the risk status of a country or zone with regard to BSE;

The Member may inform the OIE of its claimed status and the OIE may publish the claim.

and then remember this ;

IN A NUT SHELL ; $$$

(Adopted by the International Committee of the OIE on 23 May 2006)

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries.The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to then Central Bureau............

THEN, put back in place the B.S.E. G.B.R. Risk Assessments, and enhance them to include all T.S.E. i.e. the atypical strains.

REPEAL THE B.S.E. MINIMAL RISK REGION (MRR) policy !

The BSE MRR policy was shoved down the throat of every country by the O.I.E. and the U.S.D.A..

MOST every one of those Country's came down with BSE.

THE O.I.E. formula to detect B.S.E. is, and has been flawed. It was and is a policy set up for trade, NOT for human and animal health.

The BSE MRR policy made legal what the U.K. did, when the poisoned the globe with BSE. Except BSE has mutated and different strains have evolved, some that are more virulent than the c-BSE, all can transmit to humans (Kong et al 2009), all are in North America.

The BSE MRR policy was ratified while two cases of BSE were sitting on the shelf waiting to be confirmed (one was 7+ months later after an Act of Congress, and the other suspect sample that sat on a shelf for 4 months, which was not preserved correctly, which only IHC could be used, the least likely to detect BSE, was found inconclusive or negative), then the Alabama mad cow was confirmed. AFTER this, the USDA shut the testing program down to levels that would not detect BSE.

THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted products from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone. These are the facts as I have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species.

MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did, thanks to the OIE and GW, it's legal now. and they executed Saddam for poisoning ???

WHAT THE USA AND THE OIE DID, was make legal what the U.K. did when they poisoned the globe with mad cow disease. they knew what they were doing, but did it anyway. The BSE GBR risk assessments were put into place so that would never ever happen again. UNTIL they USA finally documented a case. UP until then, the USA would not accept products that may contain BSE from any country. ONCE the USA lost the 'gold card', the shoe was the on the other foot, and they literally left 2 suspect mad cow brain samples sit on a shelf for 7+ months and 4 months respectfully, all the while the BSE MRR policy was being legalized. ONCE made legal, and after an act of Congress, the one suspect Texas mad cow case that had sat up on a shelf for 7+ months was finally confirmed by Weybridge et al in the U.K., and the other, which the sample was not preserved correctly, was found after being a suspect, to be inconclusive and finally they termed it negative. Then the Alabama mad cow was confirmed and they had to shut the program down before they found anymore. ...TSS

You will recall that we have previously discussed the potential risks of BSE occurring in other countries as a result of the continuing export from the UK of meat and bone that may be contaminated by scrapie or possibly BSE.

I remain concerned that we are not being consistent in our attempts to contain the risks of BSE. Having banned the feeding of meat and bone meal to ruminamts in 1988, we should take steps to prevent these UK products being fed to ruminants in other countries. This could be achieved either through a ban on the export of meat and bone meal, or at least by the proper labelling of these products to make it absolutely clear they should not be fed to ruminants [or zoo animals, including rare and endangered primates -- webmaster]. Unless some such action is taken the difficult problems we have faced with BSE may well occur in other countries who import UK meat and bone meal. Surely it is short sighted for us to risk being seen in future as having been responsible for the introduction of BSE to the food chain in other countries.

I would be very interested to hear how you feel this gap in the present precautionary measures to eliminate BSE should be closed. We should be aiming at the global elimination of this new bovine disense. The export of our meat and bone meal is a continuing risk to other countries.

1. I spoke to Mr Capstick yesterday. Among other things, he told me that MAFF are now considering the labelling of animal foodstuffs, and in particular what detail would be required if such labelling was made compulsory. Apparently our freedom of action is constrained by EC Directives [total garbage, MAFF wants to keep exporting -- webmaster], and there is also concern about the level of detail that should be included in any foodstuff labels.

2. Mr Capstick suggested that this was not an area that DH had a particular interest. I countered by saying that we supported the principle of labelling of animal foodstuffs, particularly when these were going for export.

3. I also thanked him for keeping us informed, in a way that I hope encourage further communication of MAFF's internal deliberations.

1. SINCE the first Harvard BSE Risk Assessment was so flawed and fraught with error after the PEER REVIEW assessment assessed this fact, how do you plan on stopping this from happening again, will there be another peer review with top TSE Scientist, an impartial jury so-to-speak, to assess this new and updated Harvard BSE/TSE risk assessment and will this assessment include the Atypical TSE and SRM issues ?

Can you say TOYOTA. IT is a sad day when trade trumps human and animal health. as the case with the BSE MRR policy. Behind closed doors, the BSe spin machine is working i.e. Vilsack saying that 'The U.S. has had no cases in the last three years, and only three in two decades.' i can tell you with absolute certainty, that is only part of the story. i can tell you that in fact, the USDA BSE surveillance and testing have failed the consumer here in the USA, and abroad, and that we have been exposed to the TSE agent, i.e. USA atypical BSE, which laboratory studies show is more virulent. i can tell you with absolute certainty they infamous June 2004 enhanced BSE surveillance program, where some 800,000+ cattle were tested over many years of testing, was fraught with fraud, and in short, a failed program, and proven to be so by the GAO and the OIG, where it was proven that some of the testing program was using perfectly healthy cattle in their BSE testing program. Where some 9,200+ BSE test on suspect questionable cattle, only the IHC test were used. THE IHC is the least likely test to find BSE. IT only tells you if that part of the tissue sample is in fact infected or not, but it does not tell you about the rest of the brain. By only using the IHC, you miss many cases (Detwiler et al 2003 BSE ROUNDTABLE). i can tell you with absolute certainty, that when pressed, the USDA et al will say that even if we are missing cases of BSE, that the BSE mad cow feed ban of August 4, 1997, will stop BSE, but the ban was nothing more than ink on paper. This mad cow feed ban was only partial and voluntary. i can tell you with absolute certainty that in 2010, since 8/4/97, banned mad cow feed is in commerce here in the USA, BY THE TONS. i can tell you with absolute certainty, that when the BSE MRR policy was put in place, that this exposed everyone around the globe with the TSE agent, either by consumption and or friendly fire there from, and that decision was based NOT on science, but on trade. i can tell you with absolute certainty, that SINCE the USDA and the NSLP did in fact expose our children across the Nation with BSE via the NSLP USDA DEAD STOCK DOWNER COW SCHOOL LUNCH PROGRAM, that if they are capable of this, they are capable of exposing any person, in any country with the BSE TSE agent. North America has documented the so called typical c-BSE, l-BSE, and h-BSE. typical scrapie strains are rampant in the USA in sheep and goats, and the atypical Nor-98 scrapie is spreading, and CWD in deer and elk is spreading, with now documented a 2nd strain, and two strains of TME in mink. all this over the years have been fed back to food producing animals for animals and humans. Confucius ask, IF USA sheep Scrapie transmitted to USA cattle does not produce the same pathology as the U.K. c-BSE, why then would human CJD there from look like the U.K. nvCJD ??? what the USA has done defies all science and logic i.e. NO MAD COW DISEASE and or any human TSE there from. Either the BSE Mad Cow outbreak and human infection nvCJD there from, that happened in the U.K. was totally false, or the same thing is happening in the USA as we speak. sCJD of unknown phenotypes are rising in the USA. sporadic CJD is not a single strain, but multiple strains of unknown routes and sources of the TSE agent. IF the federal government can lie for almost a century about asbestos, and or tobacco, just to protect those two industry giants, i can guarantee you that they are doing it with mad cow type disease i.e. Transmissible Spongiform Encephalopathy. or just ask the Indians. ...TSS

DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PRIZE WINNER ON PRIONS SPEAKING ABOUT TRADE AND PRIONS, ''level of absolute ignorance'', ''yes, i think prions are bad to eat, and you can die from them''. ...(watch and turn it up)

A most interesting case, she was 38 years old, and worked a Tyson meat slaughter house, handling brain and spinal cords ;

Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas

Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas.She left 6 Kids and a Husband.The Purpose of this web is to give information in Spanish to the Hispanic community, and to all the community who want's information about this terrible disease.-

Linda was a Hispanic female with no past medical history presents with 14 months of incresing/progressive altered mental status, generalized weakness, inability to walk, loss of appetite, inability to speak, tremor and bowel/blader incontinence.She was, in her usual state of health up until February, 2009, when her husbans notes that she began forgetting things like names and short term memories. He also noticed mild/vague personality changes such as increased aggression. In March, she was involved in a hit and run MVA,although she was not injured. The police tracked her down and ticketed her. At that time, her son deployed to Iraq with the Army and her husband assumed her mentation changes were due to stress over these two events. Also in March, she began to have weakness in her legs, making it difficult to walk. Over the next few months, her mentation and personality changes worsened, getting to a point where she could no longer recognized her children. She was eating less and less. She was losing more weight. In the last 2-3 months, she reached the point where she could not walk without an assist, then 1 month ago, she stopped talking, only making grunting/aggressive sounds when anyone came near her. She also became both bowel and bladder incontinent, having to wear diapers. Her '"tremor'" and body jerks worsened and her hands assumed a sort of permanent grip position, leading her family to put tennis balls in her hands to protect her fingers.

The husband says that they have lived in Nebraska for the past 21 years. They had seen a doctor there during the summer time who prescribed her Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the medications did not help and she continued to deteriorate clinically. Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. The husband says that he does not know any fellow workers with a similar illness. He also says that she did not have any preceeding illness or travel.

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed

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The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"

Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.

Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.

Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.

An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

Methods:

12 years independent research of available data

Results:

I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

Conclusion:

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK–resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.

An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.

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Topics that will be covered in ongoing or planned reviews under Goal 1 include:

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

PLEASE be aware, for 4 years, the USDA fed our children all across the Nation dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens. who will watch our children for CJD for the next 5+ decades ???

18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.

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64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years.

***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.***

The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.

If the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. ...

Published June 14, 2010 Received for publication December 15, 2009, and accepted in revised form April 28, 2010.

Transmissible spongiform encephalopathies are lethal neurodegenerative disorders that present with aggregated forms of the cellular prion protein (PrPC), which are known as PrPSc. Prions from different species vary considerably in their transmissibility to xenogeneic hosts. The variable transmission barriers depend on sequence differences between incoming PrPSc and host PrPC and additionally, on strain-dependent conformational properties of PrPSc. The ß2-a2 loop region within PrPC varies substantially between species, with its structure being influenced by the residue types in the 2 amino acid sequence positions 170 (most commonly S or N) and 174 (N or T). In this study, we inoculated prions from 5 different species into transgenic mice expressing either disordered-loop or rigid-loop PrPC variants. Similar ß2-a2 loop structures correlated with efficient transmission, whereas dissimilar loops correlated with strong transmission barriers. We then classified literature data on cross-species transmission according to the 170S/N polymorphism. Transmission barriers were generally low between species with the same amino acid residue in position 170 and high between those with different residues. These findings point to a triggering role of the local ß2-a2 loop structure for prion transmissibility between different species.

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These observations suggest striking differences in the ß-sheet alignment of PrPSc aggregates between prion-infected 170S and 170N animals and may provide a plausible starting point for clarifying the structural basis of prion species barriers that are highly relevant to public health, including the potential transmissibility of bovine and cervid prions to humans.

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As a possible exception to these observations, cattle may be susceptible to CWD from white-tailed deer (86). The latter finding suggests that specific prion strains can overrule the codon 170 homology requirement.

About Me

My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS